To date, evoked potential work in mania has been limited although promising. The proposed study would hope to expand on our preliminary work using auditory averaged evoked responses (AER) within a conditioning testing paradigm. This work demonstrated a reversible abnormality in conditioning testing which was correlated with the degree of mania (r=.55), showing a marked reduction in suppression during acute mania, gradually improving in a subset of those patients studied as their mania improved. A separate population of euthymics, on the other hand, essentially symptom free, showed normal conditioning testing. These results suggest that a reversible defect in inhibitory pathways, specifically sensory gating, may be present in acute mania. And further, that this defect can be reflected through electrophysiological measurements, which not only might serve as a means of improving diagnosis but also as a method of more accurately monitoring the clinical state of the manic patient, an important consideration in research with affective disorders. The proposed work would hope to expand on these preliminary findings and then combine neurochemical measurements, specifically plasma and urinary levels of norepinephrine and its metabolites, MHPG and normetanephrine, purportedly increased in acute mania. Earlier work suggests neurochemical changes may correlate with electrophysiological ones. If that is true here, then a specific mechanism linking reduced sensory gating with increased norepinephrine turnover could be postulated. Briefly, the experimental design will include 20 acutely manic subjects, 20 euthymics, and 40 age and sex matched controls. Auditory AER using a conditioning testing paradigm (paired auditory clicks, 10 seconds between pairs and 0.5, 1.0, and 2.0 seconds between stimuli within the pair) will be measured on each patient. Serial measurements of AER, neurochemical parameters, and clinical ratings will be done on the acutely manic patients. Results will be analyzed looking for correlations between the degree of suppression in the AER to the test stimulus, the clinical rating of the patient and norepinephrine metabolism.